scholarly journals Knockout of secretin receptor reduces large cholangiocyte hyperplasia in mice with extrahepatic cholestasis induced by bile duct ligation

Hepatology ◽  
2010 ◽  
Vol 52 (1) ◽  
pp. 204-214 ◽  
Author(s):  
Shannon Glaser ◽  
Ian P. Lam ◽  
Antonio Franchitto ◽  
Eugenio Gaudio ◽  
Paolo Onori ◽  
...  
Keyword(s):  
Bile Duct ◽  
Bile Duct Ligation ◽  
Extrahepatic Cholestasis ◽  
Secretin Receptor ◽  
Duct Ligation

scholarly journals Vitamin A Supplementation Alleviates Extrahepatic Cholestasis Liver Injury through Nrf2 Activation

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Guiyang Wang ◽  
Peng Xiu ◽  
Fu Li ◽  
Cheng Xin ◽  
Kewei Li
Keyword(s):  
Bile Duct ◽  
Liver Injury ◽  
Liver Function ◽  
Vitamin A ◽  
Western Blotting ◽  
Bile Duct Ligation ◽  
Retinyl Palmitate ◽  
Binding Activity ◽  
Extrahepatic Cholestasis ◽  
Duct Ligation

Aim. To investigate the role of vitamin A in liver damage induced by bile duct ligation (BDL) in rats.Methods. Thirty male Wistar rats were randomly divided into three groups: SHAM group, BDL group, and BDL + VitA group . The concentrations of retinol and retinyl palmitate in the liver were analyzed using HPLC, and liver function was evaluated by the level of TBIL, ALT, AST, and ALP in serum. Hepatic oxidative status was estimated by measuring T-SOD, CAT, GSH, MDA, and AOPP. Nrf2 expression was assessed using immunohistochemistry and western blotting, and EMSA was performed to determine Nrf2 DNA-binding activity. The expression of the downstream factors such as Ho1 and Nqo1 was also examined using immunohistochemistry and western blotting assays.Results. Vitamin A treatment restored levels of retinoids in liver, improved liver function, alleviated oxidative stress, and facilitated the translocation of Nrf2 to the nucleus in the experimental obstructive jaundice. Vitamin A was also found to increase the expression of Nrf2 downstream proteins such as Ho1 and Nqo1.Conclusion. Vitamin A was here found to ameliorate cholestatic liver injury. This effect may be related to the activation of Nrf2/ARE pathway in bile duct ligation rats.

S1591 Chronic Administration of Nicotine Induces Biliary Proliferation in Both Normal and Rats with Extrahepatic Cholestasis Induced By Bile Duct Ligation (BDL)

2008 ◽  
Vol 134 (4) ◽  
pp. A-777-A-778
Author(s):  
Candace Wise ◽  
Julie Venter ◽  
Gianfranco Alpini ◽  
Bradley T. Vaculin ◽  
Shannon Glaser
Keyword(s):  
Bile Duct ◽  
Bile Duct Ligation ◽  
Chronic Administration ◽  
Extrahepatic Cholestasis ◽  
Duct Ligation

Plasma alkaline phosphodiesterase I in intrahepatic cholestasis induced by α-naphthylisothiocyanate in rats

1988 ◽  
Vol 75 (1) ◽  
pp. 13-20 ◽  
Author(s):  
Julie A. Quayle ◽  
Alison Capstick ◽  
Anthony I. Morris ◽  
David Billington
Keyword(s):  
Alkaline Phosphatase ◽  
Bile Acid ◽  
Bile Duct ◽  
Intrahepatic Cholestasis ◽  
Bile Duct Ligation ◽  
Gel Filtration ◽  
Extrahepatic Cholestasis ◽  
Rat Serum ◽  
Duct Ligation ◽  
Dose Dependent

1. Administration of α-naphthylisothiocyanate (ANIT) to rats produced dose-dependent increases in plasma bile acid and bilirubin concentrations. Similar increases in plasma bile acid and bilirubin concentrations were evident in bile duct ligated rats, indicating that the severity of cholestasis is almost identical in both models. 2. Plasma alkaline phosphodiesterase I was increased by only 50–80% while alkaline phosphatase was increased more than threefold after ANIT administration. This is in contrast to an earlier study [S. R. Simpson, K. Rahman & D. Billington (1984) Clinical Science 67, 647–652] where, after bile duct ligation, serum alkaline phosphodiesterase I was elevated sixfold before any increase in alkaline phosphatase activity became apparent. Thus, plasma alkaline phosphodiesterase I does not offer as sensitive a marker of intrahepatic cholestasis (induced by ANIT) as it does of extrahepatic cholestasis (induced by bile duct ligation). 3. Hepatic alkaline phosphodiesterase I was unaffected by ANIT pretreatment while hepatic alkaline phosphatase was increased up to seven times. It is suggested that raised plasma alkaline phosphodiesterase I is due to regurgitation of the biliary enzyme rather than overspill of the enzyme from liver into blood. 4. Gel filtration showed that 24 h and 96 h after ANIT administration, rat serum contained a high molecular weight form of alkaline phosphodiesterase I, suggesting a different isoenzyme profile.

The effects of chitosan and low dose dexamethasone on extrahepatic cholestasis after bile duct ligation in Wistar rats

2012 ◽  
Vol 99 (1) ◽  
pp. 61-73 ◽  
Author(s):  
Diana Olteanu ◽  
A. Filip ◽  
A. Mureşan ◽  
A. Nagy ◽  
F. Tabaran ◽  
...  
Keyword(s):  
Bile Duct ◽  
Wistar Rats ◽  
Low Dose ◽  
Bile Duct Ligation ◽  
Extrahepatic Cholestasis ◽  
Duct Ligation

Upregulation of secretin receptor gene expression in rat cholangiocytes after bile duct ligation

1994 ◽  
Vol 266 (5) ◽  
pp. G922-G928 ◽  
Author(s):  
G. Alpini ◽  
C. D. Ulrich ◽  
J. O. Phillips ◽  
L. D. Pham ◽  
L. J. Miller ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bile Duct ◽  
Bile Duct Ligation ◽  
Intrahepatic Bile Duct ◽  
Liver Cells ◽  
Bile Secretion ◽  
Rnase Protection ◽  
Secretin Receptor ◽  
Duct Ligation ◽  
Sr Gene

Secretion stimulates ductular bile secretion by binding to receptors on intrahepatic bile duct epithelial cells (i.e., cholangiocytes). In the rat, this choleretic effect increases after bile duct ligation (BDL). Although cholangiocyte proliferation induced by BDL contributes to secretin-induced hypercholeresis, the mechanisms modulating these alterations in secretin-induced ductular bile secretion are obscure. Thus we studied the expression of secretin receptor mRNA (SR-mRNA) in purified liver cells from normal and BDL rats. Northern blot analysis and RNase protection assays with mRNA from purified liver cells demonstrated SR-mRNA only in cholangiocytes; moreover, SR gene expression showed a seven- to ninefold increase in individual cholangiocytes from BDL rats compared with controls. This increase in SR-mRNA expression was related to a similar increase in the rate of transcription of SR-mRNA in cholangiocytes from BDL rats. Thus our studies indicate that 1) SR-mRNA is detected in liver only in cholangiocytes; 2) BDL causes an increase in SR-mRNA in individual cholangiocytes; and 3) the increase in SR-mRNA after BDL is partly related to an increase in the rate of transcription of SR-mRNA by cholangiocytes after BDL. Our data suggest that upregulation of the SR gene may contribute to secretin-induced hypercholeresis.

369 Release of Non-Neuronal Acetylcholine From Biliary Epithelial Cells During Extrahepatic Cholestasis Induced by Bile Duct Ligation

2013 ◽  
Vol 144 (5) ◽  
pp. S-943
Author(s):  
Syeda H. Afroze ◽  
Kinan Rahal ◽  
Kendal Jensen ◽  
Micheleine Guerrier ◽  
David E. Dostal ◽  
...  
Keyword(s):  
Bile Duct ◽  
Epithelial Cells ◽  
Bile Duct Ligation ◽  
Extrahepatic Cholestasis ◽  
Biliary Epithelial Cells ◽  
Duct Ligation

Bid-mediated apoptosis does not contribute to cholestatic liver injury following bile duct ligation

2009 ◽  
Vol 47 (01) ◽  
Author(s):  
P Nalapareddy ◽  
S Schüngel ◽  
MP Manns ◽  
H Jaeschke ◽  
A Vogel
Keyword(s):  
Bile Duct ◽  
Liver Injury ◽  
Bile Duct Ligation ◽  
Duct Ligation ◽  
Cholestatic Liver Injury
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